How antibiotics work

High School ・Biology ・MLA ・3 Sources

Question 1

Most of the antibiotics work by disrupting the process of integrating the peptidoglycan or the working of the ribosomes. Why the use of the cytoplasmic membranes as a point be an inefficient technique for antibacterial medicines?

The procedure involved in integrating the proteins and structure of the protein differs in the microbial (prokaryotic) and the host (eukaryotic) cells. So, utilizing the peptidoglycan synthesis or the working of the ribosome to point the bacteria is a good method. The primary structure of the cytoplasmic membrane includes a lipid, protein and the lipoprotein. The working of the cytoplasmic membrane acts as a diffusion bar for ions, water, nutrients as well as a transportation network (Gootz).

However, using the cytoplasmic membrane as a target on the bacteria is invalid because the cell membrane in both the eukaryotic and prokaryotic cell has the similar structure. Hence the antibiotic will not distinguish between the host cell and the bacteria. If the antimicrobial targeted the cytoplasmic membrane, it would affect even the host cell; it may lead to the death of host cell too. By targeting the cytoplasmic wall, the antibiotic would enter the cytoplasm and affect the processes of the mitochondria, ribosomes and the nucleus. Eventually, both cells (bacteria and host) would die due to paralyzing of the energy production and protein synthesis processes.

Question 2

A group of smokers infected with Staphylococcus aureus sues cigarettes companies. In their argument, they state that certain cigarette components affected the functioning of the phagocytes and hence influence the adverse effect of the bacteria. A microbiologist is called for court proceedings, how did she validate the claim?

Cigarette smoke consists of over 5000 chemical toxins with different effects in the human body. Both direct and second-hand cigarette smoke is the leading causative of preventable deaths as well as disabilities all over the world. The cigarette smoke inhibits the function of the phagocytes by reducing the epithelial elasticity, increasing mucus secretion, and decreasing the production of IgA. The reduction of the phagocytic functions increases the susceptibility of the respiratory system to bacterial colonization. As a result, the opportunistic infectious nasopharyngeal microflora starts to flourish. For instance, the body becomes habitable for the pathogens like the Staphylococcus aureus (Ritwij Kulkarni).

The Staphylococcus aureus, a gram-negative bacteria causes a wide range of diseases such as bacteremia, pneumonia as well as endocarditis. Unfortunately, it is costly and difficult to treat the Staphylococcus aureus infections due to the high antibacterial-resistance. Therefore, the patients spend a lot of money trying to combat the infections. The smokers have high rates of colonization by the MRSA (methicillin-resistant Staphylococcus aureus) as opposed to the nonsmokers (Elisa K. McEachern). Therefore, smoking increases the risk of Staphylococcus aureus infections as well as the difficulties in achieving the treatment. According to Kulkarni et al., the Staphylococcus aureus exposed to cigarette smoke has increased virulence due to increased biofilm formation and binding to the host cells (Elisa K. McEachern). The cigarette smoke increases the interaction between the Staphylococcus aureus and the human cells in the respiratory system. The phagocytes responsible for the elimination of foreign invaders are rendered inactive by the cigarette toxins and therefore increase the infection rates. The cigarettes companies have a stake in the prevention of the spread and infection of Staphylococcus aureus. If the cigarettes sellers fail to demonstrate to the smokers that smoking increases the risk of Staphylococcus aureus infection, they are legally liable for the problems suffered by the users (Elisa K. McEachern).

Works Cited

Elisa K. McEachern, John H. Hwang, Katherine M. Sladewski, Shari Nicatia, Carola Dewitz, Denzil P. Mathew,. "Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes." American Society for Microbiology (2015): 2443-2452 . Print.

Gootz, Harold C. Neu and Thomas D. "Antimicrobial Chemotherapy." NCBI (1996): 2-5. Print.

Ritwij Kulkarni, Swati Antala, Alice Wang, Fábio E. Amaral, Ryan Rampersaud, Samuel J. LaRussa, Paul J. Planet, Adam J. Ratne. "Cigarette Smoke Increases Staphylococcus aureus Biofilm Formation via Oxidative Stress." NCBI (2012): 3804–3811. Print.

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